Recently, the known compound (-)-3-(3,4-dihydroxyphenyl)-L-alanine, (L-dopa) was found useful in the symptomatic treatment of parkinsonism. The use of L-dopa for such treatment was prompted by the finding that a relationship existed between the above-mentioned classical abnormalities and a biochemical deficiency of dopamine; it being known that certain enzymes were capable of converting L-dopa to dopamine. Thus, it was rationalized that the administration of L-dopa should increase the body's supply of dopamine and reduce the symptoms of Parkinsonism. The hypothesis was tested and proved valid. Since the observed therapeutic effect was believed to be due to the increased supply of dopamine, it was also reasoned that the administration of dopamine should also result in a reduction of the symptoms of Parkinsonism. Surprisingly, dopamine itself was found to be substantially ineffective in the treatment of such symptoms. Thus it is postulated that free dopamine is not transported across the blood-brain barrier and, therefore, does not give symptomatic relief. This being the case, it is surprising that certain amides of dopamine and of other substituted phenylamines exhibit such an effect.